This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Chlamydia trachomatis, the most common cause of bacterial sexually transmitted infection, has been linked to cervical cancer in epidemiologic studies. This association may involve effects of a chlamydial infection on the centrosome that are characterized by dysregulation of centrosome duplication and appearance of multiple centrosomal foci. However, these centrosome abnormalities have not been analyzed at an ultrastructural level. We have found that the centrosomal regulator HsSAS-6 is proteolytically modified during a chlamydial infection. HsSAS-6 is cleaved, producing stable cleavage products that are sufficient to cause centrosome amplification. It is our goal to determine on an ultrastructural level whether proteolytic effects on HsSAS-6 are sufficient to cause the amplified centrosome phenotype of Chlamydia-infected cells.